C-Reactive Protein (CRP) is an acute phase protein in man that incrases as much as several hundred fold during acute pathological conditions. Previous investigations indicate that the CRP found on Natural Killer (NK) cells is not passively acquired, we will determine how cell surface CRP is acquired. There is a subpopulation of mononuclear cells that bind ligand complexed CRP and a similar percentage that bind CRP. The mononuclear cells that bind CRP ligand complexes are morphologically similar to the NK cells. Both are LGL, both hve IgG FcR and both form weak rosetts with SRBC. However, addition of exogenous CRP:CPS complexes does not alter the function or number of NK effectors. Recent investigations indicate that anti-CRP and complement removes NK function, which suggests that CRP or an antigenically similar molecule is present on NK effector cells. Our initial goals in these studies are to verify that CRP itself is present on NK cells, that it is a unique marker for NK effector cells, and that CRP is required for an NK response. We will subsequently investigate the role CRP plays in NK mediated killing. We further propose exploration of the CRP-bearing and CRP-binding lymphocytes in normal vs turmor-bearing patients. If a direct correlation can be made between the cells and if the levels of CRP-bearing and CRP-binding cells are elevated during the acute phase response, this would support a role of NK cells in defense against malignancy which could lead to methods for regulation of these vital effectors.